title: Inhibition of androgen induces autophagy in benign prostate epithelial cells.
abstract: OBJECTIVE
  5-α Reductase inhibitor can reduce the volume of benign prostatic hyperplasia by lowering benign prostatic hyperplasia level and consequently inducing epithelial cells apoptosis. The present study investigated whether autophagy and apoptosis of benign prostatic hyperplasia epithelial cells are influenced by low benign prostatic hyperplasia levels.
  
  
  METHODS
  PWR-1E prostate epithelial cells transfected with GFP-LC3 plasmid were subjected to androgen deprivation conditions. Then the autophagic puncta were evaluated by fluorescence microscopy, and the cellular apoptosis rate was detected by 4, 6-diamidino-2-phenylindole staining after blocking of autophagic process by 3-methyladenine. Furthermore, autophagy status was also determined in hyperplasia prostate tissues from 5-α reductase inhibitor-treated patients by immunohistochemistry.
  
  
  RESULTS
  In the androgen deprivation medium, autophagic punta increased markedly in PWR-1E cells, and blockage of autophagy by 3-methyladenine significantly promoted PWR-1E cells' apoptosis rate. In vivo, the expression of LC3 protein (an important autophagic marker) in hyperplasia prostate tissue significantly increased after 5-α reductase inhibitor treatment. Meanwhile, the prostate-specific antigen, as an inner control, decreased.
  
  
  CONCLUSIONS
  5-α Reductase inhibitor treatment increases autophagy and possibly decreases the apoptosis of prostate epithelial cells.
authors.affiliation: Department of Urology, Union Hospital of Fujian Medical University, Fuzhou, China.
authors.forename: Mengqiang
authors.initials: M
authors.lastname: Li
authors.forename: Xu
authors.initials: X
authors.lastname: Yang
authors.forename: Huili
authors.initials: H
authors.lastname: Wang
authors.forename: Enci
authors.initials: E
authors.lastname: Xu
authors.forename: Zhijun
authors.initials: Z
authors.lastname: Xi
mesh_terms: D058891:5-alpha Reductase Inhibitors / Q000494:pharmacology; D000368:Aged; D000369:Aged, 80 and over; D000728:Androgens / Q000378:metabolism*; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D001343:Autophagy / Q000502:physiology*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D013196:Dihydrotestosterone / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D018120:Finasteride / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011467:Prostate / Q000166:cytology*; D011470:Prostatic Hyperplasia / Q000188:drug therapy / Q000473:pathology*
chemical_list: D058891:5-alpha Reductase Inhibitors; D000728:Androgens; D013196:Dihydrotestosterone; D018120:Finasteride
keywords: 5-α reductase inhibitor; autophagy; benign prostatic hyperplasia; dihydrotestosterone